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Tumorigenicity of 5-Methylchrysene Dihydrodiols and Dihydrodiol Epoxides in Newborn Mice and on Mouse Skin¹

Naylor Dana Institute for Disease Prevention, American Health Foundation, Valhalla, New York 10595 [S. S. H., L. R., S. A., K. H., A. A. M., D. H.], and The Ben May Laboratory for Cancer Research, University of Chicago, Chicago, Illinois 60637 [J. P., R. G. H.]

5-Methylchrysene, (±)-trans-1,2-dihydro-1,2-dihydroxy-5-methylchrysene, (±)-trans-7,8-dihydro-7,8-dihydroxy-5-methylchrysene, (±)-trans-1,2-dihydroxy-anti-3,4-epoxy-1,2,3,4-tetrahydro-5-methylchrysene (anti-DE-I), (±)-trans-1,2-dihydroxy-syn-3,4-epoxy-1,2,3,4-tetrahydro-5-methylchrysene (syn-DE-I), and (±)-trans-7,8-dihydroxy-anti-9,10-epoxy-7,8,9,10-tetrahydro-5-methylchrysene (anti-DE-II) were tested for tumorigenicity in newborn mice and for tumor-initiating activity on mouse skin. In newborn mice, a total dose of 56 nmol of anti-DE-I induced 4.6 lung tumors/mouse and 1.2 liver tumors/mouse. These incidences were significantly higher than observed for any of the other metabolites, tested at equimolar doses. The results indicate that anti-DE-I, but not syn-DE-I or anti-DE-II, is a major ultimate carcinogen of 5-methylchrysene in the newborn mouse. Anti-DE-I was also more tumorigenic than anti-DE-II on mouse skin, inducing 4.4 tumors/mouse after an initiating dose of 100 nmol, compared to zero tumors per mouse induced by anti-DE-II. However, anti-DE-I was less tumorigenic on mouse skin than was its metabolic precursor, trans-1,2-dihydro-1,2-dihydroxy-5-methylchrysene or its parent hydrocarbon, 5-methylchrysene.

¹ This study was supported by Grant CA 32242 from the National Cancer Institute. This is Paper 79 of the series, "A Study of Chemical Carcinogenesis."

² To whom requests for reprints should be addressed.

Received 9/ 4/84. Revised 12/ 4/84. Accepted 12/ 6/84.